The aim of this research proposal is to study the pathogensis of hypertension produced by glucocorticosteroids in the rat. Prior studies had suggested that glucocorticoid hypertension was different from that due to mineralocorticoids in that excessive salt intake was not required for cortisone to produce high blood pressure. The applicant has already shown that glucorticoids can produce increased plasma renin activity and plasma renin substrate in man. Preliminary studies indicate that the synthetic steroid, methylprednisolone, elevates the arterial pressure of the rat and leads to similar derangements of the renin-angiotensin system. In addition, selective supersensitivity to angiotensin II in the glucocorticoid treated rat is suggested. It is proposed that precise measurements of arterial pressure, plasma renin concentration, plasma renin activity and plasma renin substrate be carried out in close correlation with measured changes in sodium balance in glucocorticoid treated rats. In addition arterial pressure sensitivity to angiotensin II and te response to an angiotensin antagonist (1-Sar 8-ala- angiotensin II) are to be carried out. The results of these studies may bear on the pathogenesis of hypertension in Cushing's Syndrome and that associated with glucocorticoid therapy - especially in the area of the treatment of chronic glomeruler diseases and of renal transplant patients.